Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows. - Test2 - elhamkhani - TriplyDB

Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.

Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.

http://www.wikidata.org/entity/Q34278418

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Rett Syndrome: Crossing the Threshold to Clinical Translation Excitatory/Inhibitory Balance and Circuit Homeostasis in Autism Spectrum Disorders MeCP2 post-translational modifications: a mechanism to control its involvement in synaptic plasticity and homeostasis?Rett syndrome: disruption of epigenetic control of postnatal neurological functions Methyl-CpG binding protein 2 (MeCP2) localizes at the centrosome and is required for proper mitotic spindle organization MECP2 regulates cortical plasticity underlying a learned behaviour in adult female mice Beyond Widespread Mecp2 Deletions to Model Rett Syndrome: Conditional Spatio-Temporal Knockout, Single-Point Mutations and Transgenic Rescue Mice Preclinical research in Rett syndrome: setting the foundation for translational success.The neural circuit basis of Rett syndrome Functional recovery with recombinant human IGF1 treatment in a mouse model of Rett Syndrome.Systemic delivery of MeCP2 rescues behavioral and cellular deficits in female mouse models of Rett syndrome MeCP2 dependent heterochromatin reorganization during neural differentiation of a novel Mecp2-deficient embryonic stem cell reporter line.Gait analysis in a Mecp2 knockout mouse model of Rett syndrome reveals early-onset and progressive motor deficits Mouse models of neurodevelopmental disease of the basal ganglia and associated circuits.The molecular basis of variable phenotypic severity among common missense mutations causing Rett syndrome Human-specific regulation of MeCP2 levels in fetal brains by microRNA miR-483-5p.NMDA receptor regulation prevents regression of visual cortical function in the absence of Mecp2.Acute and crucial requirement for MeCP2 function upon transition from early to late adult stages of brain maturation Loss of MeCP2 function is associated with distinct gene expression changes in the striatum Breathing challenges in Rett syndrome: lessons learned from humans and animal models.Oligodendrocyte lineage cells contribute unique features to Rett syndrome neuropathology Rescue of behavioral and EEG deficits in male and female Mecp2-deficient mice by delayed Mecp2 gene reactivation.From Function to Phenotype: Impaired DNA Binding and Clustering Correlates with Clinical Severity in Males with Missense Mutations in MECP2.Loss of MeCP2 from forebrain excitatory neurons leads to cortical hyperexcitation and seizures.Synaptic plasticity and signaling in Rett syndrome.Rett syndrome: a complex disorder with simple roots.Defects During Mecp2 Null Embryonic Cortex Development Precede the Onset of Overt Neurological Symptoms.The 3' UTR of FMR1 mRNA is a target of miR-101, miR-129-5p and miR-221: implications for the molecular pathology of FXTAS at the synapse.Radically truncated MeCP2 rescues Rett syndrome-like neurological defects.Selective preservation of MeCP2 in catecholaminergic cells is sufficient to improve the behavioral phenotype of male and female Mecp2-deficient mice.Expression of Phospho-MeCP2s in the Developing Rat Brain and Function of Postnatal MeCP2 in Cerebellar Neural Cell Development.Conditional depletion of methyl-CpG-binding protein 2 in astrocytes depresses the hypercapnic ventilatory response in mice.A mutation-led search for novel functional domains in MeCP2.

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P2860

Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.

http://www.wikidata.org/entity/Q34278418

description

2012 nî lūn-bûn

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2012 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2012 թվականի մայիսին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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name

Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.

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Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.

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Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.

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type

label

Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.

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Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.

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Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.

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prefLabel

Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.

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Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.

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Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.

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P1433

Human Molecular Genetics

P1476

Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.

@en

P2093

Adrian Bird

http://www.w3.org/2001/XMLSchema#string

Cara Merusi

http://www.w3.org/2001/XMLSchema#string

Dina De Sousa

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Hélène Cheval

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Jacky Guy

http://www.w3.org/2001/XMLSchema#string

Jim Selfridge

http://www.w3.org/2001/XMLSchema#string

P2860

Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2

Phenotypic manifestations of MECP2 mutations in classical and atypical Rett syndrome

The story of Rett syndrome: from clinic to neurobiology

Purification, sequence, and cellular localization of a novel chromosomal protein that binds to methylated DNA

A mouse Mecp2-null mutation causes neurological symptoms that mimic Rett syndrome

MECP2 is progressively expressed in post-migratory neurons and is involved in neuronal maturation rather than cell fate decisions

A partial loss of function allele of methyl-CpG-binding protein 2 predicts a human neurodevelopmental syndrome

Developmental expression of methyl-CpG binding protein 2 is dynamically regulated in the rodent brain

Regional differences in synaptogenesis in human cerebral cortex

Deficiency of methyl-CpG binding protein-2 in CNS neurons results in a Rett-like phenotype in mice

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3806-3814

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scholarly article

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10.1093/HMG/DDS208

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17

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21

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225088309

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22653753

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3412380

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